Staphylococcus epidermidis induced toxic shock syndrome (TSS) secondary to influenza infection.

BACKGROUND: To date, few cases of TSS caused by coagulase negative (CoN) staphylococci have been reported in the literature. Recent data show that CoN staphylococci are capable of secreting a number of enterotoxins and cytotoxins, normally produced by S. aureus. Herewith, we describe a case of TSS caused by Staphylococcus epidermidis with a favorable outcome. CASE PRESENTATION: We report a case of a 46-year-old man who developed TSS from S. epidermidis. The patient was admitted for a 7-day history of general malaise and headache following a recent influenza infection and a 3-day history of vomiting, diarrhea, diffuse erythroderma, and fever. The main laboratory findings on admission were leukopenia (WBC 800/mm3), thrombocytopenia (Plt count 78.000/mm3), elevated urea, creatine levels and increased inflammatory markers (CRP 368 mg/ml). The patient had clinical and radiological evidence of pneumonia with chest computed tomography (CT) showing diffuse bilateral airspace opacifications with air bronchogram. On the second day, a methicillin resistant S. epidermidis (MRSE) strain was detected in both sets of blood cultures, but the organism was unavailable for toxin testing. All other cultures and diagnostic PCR tests were negative. His clinical signs and symptoms fulfilled at that stage four out of five clinical criteria of TSS with a fever of 39 °C, diffuse erythroderma, multisystem involvement and hypotension. On the same day the patient was admitted to the ICU due to acute respiratory failure. The initial treatment was meropenem, vancomycin, levofloxacin, clindamycin, IVIG and steroids. Finger desquamation appeared on the 9th day of hospitalization, fulfilling all five clinical criteria for TSS. CONCLUSIONS: To our knowledge, this is the first adult case with TSS induced by CoNS (MRSE) secondary to an influenza type B infection, who had favorable progression and outcome. Further research is warranted to determine how TSS is induced by the CoNS infections.

Physiologic effects of stress dose corticosteroids in in-hospital cardiac arrest (CORTICA): A randomized clinical trial.

Aim: Postresuscitation hemodynamics are associated with hospital mortality/functional outcome. We sought to determine whether low-dose steroids started during and continued after cardiopulmonary resuscitation (CPR) affect postresuscitation hemodynamics and other physiological variables in vasopressor-requiring, in-hospital cardiac arrest. Methods: We conducted a two-center, randomized, double-blind trial of patients with adrenaline (epinephrine)-requiring cardiac arrest. Patients were randomized to receive either methylprednisolone 40 mg (steroids group) or normal saline-placebo (control group) during the first CPR cycle post-enrollment. Postresuscitation shock was treated with hydrocortisone 240 mg daily for 7 days maximum and gradual taper (steroids group), or saline-placebo (control group). Primary outcomes were arterial pressure and central-venous oxygen saturation (ScvO2) within 72 hours post-ROSC. Results: Eighty nine of 98 controls and 80 of 86 steroids group patients with ROSC were treated as randomized. Primary outcome data were collected from 100 patients with ROSC (control, n = 54; steroids, n = 46). In intention-to-treat mixed-model analyses, there was no significant effect of group on arterial pressure, marginal mean (95% confidence interval) for mean arterial pressure, steroids vs. control: 74 (68-80) vs. 72 (66-79) mmHg] and ScvO2 [71 (68-75)% vs. 69 (65-73)%], cardiac index [2.8 (2.5-3.1) vs. 2.9 (2.5-3.2) L/min/m2], and serum cytokine concentrations [e.g. interleukin-6, 89.1 (42.8-133.9) vs. 75.7 (52.1-152.3) pg/mL] determined within 72 hours post-ROSC (P = 0.12-0.86). There was no between-group difference in body temperature, echocardiographic variables, prefrontal blood flow index/cerebral autoregulation, organ failure-free days, and hazard for poor in-hospital/functional outcome, and adverse events (P = 0.08->0.99). Conclusions: Our results do not support the use of low-dose corticosteroids in in-hospital cardiac arrest.Trial Registration:ClinicalTrials.gov number: NCT02790788 ( https://www.clinicaltrials.gov ).